Induction of apoptosis by deinoxanthin in human cancer cells
Yong-Ji Choi1, Jung-Mu Hur, Sangyong Lim
1Department of Biotechnology and Bioengineering, Chonnam National University, Gwangju 500-757, South Korea. choiji01@jnu.ac.kr.
Background:
Deinoxanthin is unique carotenoid isolated from the radioresistant bacterium Deinococcus radiodurans. In the present study, the induction of apoptosis of cancer cells by deinoxanthin was investigated.
Materials And Methods:
Apoptotic effects were evaluated in HepG2, PC-3, and HT-29 cells, and were measured through cell viability, morphological changes, and a DNA fragmentation assay. Intracellular generation of reactive oxygen species (ROS) was measured using 5-(and 6-)-carboxy-2',7'-dichlorodihydrofluorescein diacetate (carboxy-H2DCF-DA). The expression of apoptotic and anti-apoptotic proteins was assayed by western blotting.
Results:
The half-maximal inhibitory concentration (IC50) values for deinoxanthin against the HepG2, HT-29, and PC-3 cell lines were 59 μM, 61 μM, and 77 μM, respectively. Deinoxanthin treatment caused an increase in ROS in all tested cells, suggesting possible pro-oxidant activity of deinoxanthin. Pro-caspase-3 was degraded in cancer cells by deinoxanthin treatment. Moreover, BCL2 expression decreased, but that of BAX increased.
Conclusion:
The present findings demonstrate for the first time the novel functional property of deinoxanthin isolated from radioresistant bacteria as a potent inducer of apoptosis in cancer cells. These data suggest that deinoxanthin could be potentially useful as a chemopreventive agent.
Insights
Deinoxanthin, a carotenoid from Deinococcus radiodurans, effectively induces apoptosis in cancer cells by increasing reactive oxygen species (ROS) and altering apoptotic protein expression. This suggests its potential as a chemopreventive agent.
Area of Science:
- Biochemistry
- Cell Biology
- Microbiology
Background:
- Deinoxanthin is a unique carotenoid derived from the radioresistant bacterium Deinococcus radiodurans.
- Its potential role in inducing cancer cell apoptosis has not been previously explored.
Purpose of the Study:
- To investigate the apoptosis-inducing effects of deinoxanthin on various cancer cell lines.
- To elucidate the underlying mechanisms, including reactive oxygen species (ROS) generation and apoptotic protein modulation.
Main Methods:
- Evaluated apoptotic effects in HepG2, PC-3, and HT-29 cells using assays for cell viability, morphology, and DNA fragmentation.
- Measured intracellular ROS generation using carboxy-H2DCF-DA.
- Assayed apoptotic and anti-apoptotic protein expression via western blotting.
Main Results:
- Deinoxanthin exhibited half-maximal inhibitory concentrations (IC50) of 59 μM (HepG2), 61 μM (HT-29), and 77 μM (PC-3).
- Treatment increased ROS levels in all tested cancer cells, indicating potential pro-oxidant activity.
- Deinoxanthin treatment led to pro-caspase-3 degradation and altered BCL2/BAX expression ratios, favoring apoptosis.
Conclusions:
- This study demonstrates deinoxanthin's novel function as a potent inducer of apoptosis in cancer cells.
- The findings suggest deinoxanthin holds promise as a potential chemopreventive agent.
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